Overview: Rhinovirus is a
single-stranded, positive-sense RNA virus that
possesses a naked (as opposed to enveloped)
icosahedral assembly of 60 protomers (Figure
1).
There are 100 recognized serotypes of this
particular virus, making it the most common
viral agent in humans, and a causative agent of
the common cold. Due to its small size and
diameter of about 30 nm, this pathogen's genome
is approximately 7.2 to 8.2 kilobases in length
and possesses a virus encoded protein at its 5’
(five prime)
end and a poly(A)-tail at its 3' end. The capsid
is composed of four viral proteins: VP1, VP2,
VP3, and VP4. The viral proteins VP1, VP2, and
VP3 are epitopes that interact with antibodies
of the host's immune system (Larralde et al.,
1991).

Figure 1. A
graphical representation of rhinovirus.

Pathogenicity:
Rhinovirus can be transmitted
by two methods, namely, via respiratory droplets and
from contaminated surfaces, including direct
person-to-person contact (Figure
2). The primary
method of entrance into the body is through the
nasal mucosa. Optimal
replication of rhinovirus occurs between
33°C to 35°C; this is why viral replication
occurs best in the nasal passages and upper
tracheobronchial trees, as opposed to the lower
respiratory tract, which is close to 37°C.

Figure 2.
This photograph demonstrates a sneeze in
progress, revealing the plume of salivary
droplets as they are expelled in a large
cone-shaped array from this man’s open mouth,
thereby, dramatically illustrating the reason
one needs to cover his/her mouth when coughing,
or sneezing, in order to protect others from
germ exposure.

When a rhinovirus virion
first encounters targeted epithelial cells of
the upper respiratory tract, it attaches to
intracellular adhesion molecule-1 (ICAM-1) on
respiratory epithelium via VP1 and enters by
endocytosis (Figure
3). Viral RNA is then synthesized and
translated into VP1 through VP4. Since the virus
initially contains a positive-sense RNA strand
as its genome, the RNA is used as a template to
produce a negative-sense RNA strand. This is
done using viral replicase, an enzyme which is
usually carried in the nucleoprotein core. The
negative-sense strand is subsequently used as a
template to generate many strands of
positive-sense RNA, as the genome for progeny
virions being produced (Figure
4). The assembly of viral proteins and RNA
creates new virions that exit the infected
cell by lysis and spread locally to
invade neighboring cells. The replication cycle
of rhinovirus is summarized in
Figure 5.

Figure 3.
The attachment of rhinovirus capsid proteins to
target cell membrane proteins. The crevice in
which the membrane protein fits into is called
the 'canyon'.

Figure 4.
Overview of viral replication strategies.
Click to enlarge.

Figure 5.
Structure & replication cycle of rhinovirus.

Symptoms of
Infection: Incubation periods last about two to four days.
Inflammatory responses caused by rhinovirus in
the respiratory tract can lead to:

Nasal discharge

Nasal congestion

Sneezing

Throat irritation

Edema and erythema of
nasal mucosae may be present

At the moment, there is no
true vaccine or treatment available to prevent
or treat infections associated with the virus,
other than a few antiviral drugs that inhibit
viral RNA from being injected into the host,
such as pleconaril (Heikkinen et al.,
2003) . Research conducted by Larralde et al.
(1991) showed that even though there are many
serotypes of rhinovirus, similarities in the VP4
protein give hope for future vaccines.